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To explore the efficacy and mechanism of Pomegranate peel Ginger ultrafine powder (PG) in treating chronic enteritis in mice. Sixty SPF-grade mice were randomly divided into a blank group, a model group, loperamide hydrochloride group (5 mg/kg), a high-dose PG group (100 mg/kg), a medium-dose group (50 mg/kg), and a low-dose group (25 mg/kg), with 10 mice in each group and an equal number of males and females. A chronic enteritis mouse model was established using a multifactorial method of low temperature + ice water + castor oil. The blank group was given an equal amount of physiological saline intragastrically, while the other groups were intervened with corresponding drugs for 7 consecutive days. After 7 days, samples were collected, and Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleuckin 1β (IL-1β), IL-6, and Tumor necrosis factorα(TNF-α) in mouse serum. HE staining was used to examine the pathological changes in the small intestine. oxidative reagent kits were used to detect the content of total superoxide dismutase(T-SOD) and Malondialdehyde (MDA) in the small intestine. Western blot was used to detect the expression of Aquaporin 8(AQP8) proteins in the small intestine. Real time quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to detect the expression of AQP3, AQP4, AQP8, and Sodium/hydrogen exchanger 8 (NHE8) genes in the small intestine. metagenomics was used to detect the gut microbiota in mouse feces. Compared with the model group, all doses of PG groups reduced the levels of IL-1β, IL-6, and TNF-α in mouse serum (P<0.05), improved pathological changes in the small intestine, increased the content of T-SOD in the small intestine tissue, reduced the content of MDA, increased the expression of AQP4 and AQP8 mRNA, and decreased the expression of AQP3 and NHE8 mRNA (P<0.05), increased the expression of AQP8 protein. PG could improve the pathological changes of chronic enteritis in mice, enhance antioxidant capacity, and alleviate diarrhea caused by chronic enteritis by downregulating the expression of intestinal epithelial transport proteins and acute-phase proteins, and altering gut microbiota.

Malabsorption of NaCl is the primary cause of diarrhea in inflammatory bowel disease (IBD). Coupled NaCl absorption occurs via the dual operation of Na:H and Cl:HCO3 exchange in the brush border membrane (BBM) of villus cells. Cl:HCO3 exchange is mediated by BBM transporters DRA (downregulated in adenoma) and PAT1 (putative anion transporter 1) in the mammalian small intestine. DRA/PAT1-mediated Cl:HCO3 exchange was significantly downregulated in the BBM of villus cells in a rabbit model of chronic ileitis, while Na:H exchange was unaffected. The inhibition of Cl:HCO3 exchange was restored in the rabbits when treated with a broad-spectrum immunomodulator, i.e. a glucocorticoid, indicating that the downregulation of DRA/PAT1 is likely to be immune-mediated during chronic enteritis. Mucosal mast cells are one type of key immune cells that are known to proliferate and release immune inflammatory mediators, thus playing a significant role in the pathogenesis of IBD. However, how mast cells may regulate DRA- and PAT1-mediated Cl:HCO3 exchange in a rabbit model of chronic ileitis is unknown. In this study, treatment of rabbits with chronic intestinal inflammation with the mast cell stabilizer ketotifen did not affect the mucosal architecture of the inflamed intestine. However, ketotifen treatment reversed the inhibition of Cl:HCO3 activity in the BBM of villus cells. This restoration of Cl:HCO3 activity to normal levels by ketotifen was found to be secondary to restoring the affinity of the exchangers for its substrate chloride. This observation was consistent with molecular studies, where the mRNA and BBM protein expressions of DRA and PAT1 remained unaffected in the villus cells under all experimental conditions. Thus, this study indicates that mast cells mediated the inhibition of coupled NaCl absorption by inhibiting Cl:HCO3 exchange in a rabbit model of chronic enteritis.

IntroductionColorectal cancer (CRC) remains an incurable disease. Previous metabolomic studies show that metabolic signatures in plasma distinguish CRC patients from healthy controls. Chronic enteritis (CE) represents a risk factor for CRC, with a 20 fold greater incidence than in healthy individuals. However, no studies have performed metabolomic profiling to investigate CRC biomarkers in CE.ObjectiveOur aims were to identify metabolomic signatures in CRC and CE and to search for blood-derived metabolite biomarkers distinguishing CRC from CE, especially early-stage biomarkers.MethodsIn this case–control study, 612 subjects were prospectively recruited between May 2015 and May 2016, and including 539 CRC patients (stage I, 102 cases; stage II, 259 cases; stage III, 178 cases) and 73 CE patients. Untargeted metabolomics was performed to identify CRC-related metabolic signatures in CE.ResultsFive pathways were significantly enriched based on 153 differential metabolites between CRC and CE. 16 biomarkers were identified for diagnosis of CRC from CE and for guiding CRC staging. The AUC value for CRC diagnosis in the external validation set was 0.85. Good diagnostic performances were also achieved for early-stage CRC (stage I and stage II), with an AUC value of 0.84. The biomarker panel could also stage CRC patients, with an AUC of 0.72 distinguishing stage I from stage II CRC and AUC of 0.74 distinguishing stage II from stage III CRC.ConclusionsThe identified metabolic biomarkers exhibit promising properties for CRC monitoring in CE patients and are superior to commonly used clinical biomarkers (CEA and CA19-9).

Edwardsiella tarda is a zoonotic facultative intracellular bacterium whose impact on farm-raised amphibians is still poorly defined. We recovered seven strains from American bullfrogs (Aquarana catesbeiana) on four farms in Guangdong, China, and combined field surveillance with molecular and pathological investigations. Phylogenetic analysis of 16S rRNA and rpoB sequences confirmed species identity. Quantitative PCR of 192 apparently healthy frogs revealed intestinal carriage at every farm, with prevalence ranging from 39 to 77 percent and bacterial loads of 105–106 CFU/mL, indicating widespread subclinical colonisation. Virulence profiling demonstrated a conserved core gene set (gadB, mukF, citC, fimA, ompA) and accessory variation confined to the flagellar gene fliC. The strains resisted trimethoprim, ampicillin, and tetracyclines, yet remained susceptible to third generation cephalosporins, carbapenems, and most aminoglycosides. Infection trials showed that although very high inocula caused acute fatalities, an inoculum of 108 CFU/mL was sufficient to induce persistent enteritis characterised by suppressed tight junction proteins, elevated cytokine expression, and marked intestinal damage. These findings demonstrate that E. tarda circulates silently in bullfrog culture, carries an amphibian adapted virulence profile and still responds to key antimicrobials, providing a baseline for risk assessment, surveillance, and targeted control in amphibian aquaculture.

The pathologic, molecular, and immunohistochemical findings associated with Neorickettsia helminthoeca are described in coatis (Nasua nasua). Tissue sections (small intestine, lungs, kidney, liver, and spleen) of coatis (n = 3) that died at the Bela Vista Biological Refuge, Foz do Iguaçu, Paraná, southern Brazil were routinely processed from histopathology. Selected formalin-fixed paraffin-embedded (FFPE) tissue sections of the small intestine, lungs, and spleen were used in an immunohistochemical (IHC) assay designed to identify the antigens of N. helminthoeca. Additionally, FFPE tissue sections of the small intestine were used to demonstrate antigens of canine parvovirus-2 (CPV-2) by IHC. Histopathology revealed chronic enteritis in all coatis. Parasitic enteritis was diagnosed in two coatis; one of these contained examples of a trematode within the lumen of the small intestine and the ovum of a trematode encysted in the intestinal mucosa. Other significant pathologic findings included interstitial pneumonia (n = 2) and pyogranulomatous splenitis (n = 1). Positive immunolabeling for N. helminthoeca was identified within macrophages of the small intestine and reticuloendothelial cells within the germinal centers of the spleen of all coatis; the intestinal trematode was N. helminthoeca IHC-positive. All pulmonary sections revealed negative immunolabeling for N. helminthoeca. Furthermore, the antigens of CPV-2 were not identified in the intestine of any coati. These findings indicate that these coatis were infected by N. helminthoeca, but since clinical and gross pathological findings were not recorded, it is uncertain if this pathogen produced clinical disease in this canid host; therefore, coatis may be asymptomatic or dead-end hosts for this organism.

After an incubation period of weeks to months, up to 14% of cats infected with feline coronavirus (FCoV) develop feline infectious peritonitis (FIP): a potentially lethal pyogranulomatous perivasculitis. The aim of this study was to find out if stopping FCoV faecal shedding with antivirals prevents FIP. Guardians of cats from which FCoV had been eliminated at least 6 months earlier were contacted to find out the outcome of their cats; 27 households were identified containing 147 cats. Thirteen cats were treated for FIP, 109 cats shed FCoV and 25 did not; a 4–7-day course of oral GS-441524 antiviral stopped faecal FCoV shedding. Follow-up was from 6 months to 3.5 years; 11 of 147 cats died, but none developed FIP. A previous field study of 820 FCoV-exposed cats was used as a retrospective control group; 37 of 820 cats developed FIP. The difference was statistically highly significant (p = 0.0062). Cats from eight households recovered from chronic FCoV enteropathy. Conclusions: the early treatment of FCoV-infected cats with oral antivirals prevented FIP. Nevertheless, should FCoV be re-introduced into a household, then FIP can result. Further work is required to establish the role of FCoV in the aetiology of feline inflammatory bowel disease.

The report describes a case of urogenital myiasis in a domestic rabbit Oryctolagus cuniculus L. (Lagomorpha: Leporidae) caused by Lucilia sericata (Meigen; Diptera: Calliphoridae) in region Emilia-Romagna (Northern Italy). The case, occurring in June 2018, is the first one involving L. sericata as an agent of myiasis in a domestic rabbit in Italy. Species identification was based on morphological investigations of males through identification keys. The rabbit developed the urogenital myiasis as a consequence of chronic enteritis causing an accumulation of faeces in the perianal and perineal region.

Background Diagnosing IBD in horses is challenging and requires a multimodal approach, since no conclusive diagnostic test is available. The objectives of this study were to provide an overview of population characteristics, results of applied diagnostic tests, treatment modalities and outcome in a large group of horses thought to have IBD and that were presented to four large equine referral hospitals, and to provide an exploratory investigation of possible associations between results of applied diagnostic tests, applied treatment modalities and outcome. A retrospective case series was performed across four large equine referral hospitals. Seventy-eight horses, thought to have IBD were included. Case history, clinical findings, diagnostic test results including oral glucose tolerance test (OGTT) and enteral biopsies (both duodenal and rectal), applied therapy and outcome were studied. A Chi-Square test was used to identify associations between results of diagnostic tests, treatment and outcome. P -values < 0.05 were considered significant. Results Lethargy, diarrhoea, recurrent colic and weight loss were recorded in respectively 21,8%; 14,1%; 28,2% and 78,2% of cases. Over 70% of horses thought to have IBD had an abnormal OGTT. Only weight loss was significantly associated with aberrant enteral biopsy results, but not with abnormal OGTT results or low blood total protein. There was no association between an aberrant biopsy result and a disturbed OGTT. There was no association between either OGTT results or enteral biopsy results and a low blood total protein content, presence of gastric ulcer disease or an aberrant endoscopic aspect of the duodenal entrance. Conclusions Weight loss is a highly prevalent symptom in IBD suspected horses. Enteral biopsies may be a useful diagnostic aid in the work-up of horses thought to suffer from IBD, however further research is required to demonstrate their true diagnostic value. Until more standardized scientific research is available, one should be careful with the interpretation of enteral biopsy results There is a need for better standardization of enteral biopsy procedures and the histopathological scoring of biopsies.

Glutamine has been proposed as a preventive treatment for toxicity related to cancer therapies. The aim of this study was to test the efficacy of glutamine in the prevention of radiation enteritis. A randomized, double-blind, controlled trial was performed including 69 patients who were assigned to receive either glutamine (Gln, 30 g/d) or placebo while they were receiving abdominal radiotherapy. Patients were re-evaluated 1 y after completion of treatment. The presence of chronic enteritis was assessed using the Radiation Therapy Oncology Group scale. Nutritional status was evaluated using subjective global assessment, weight, and bioimpedance. Relative risk (RR) and its confidence interval (CI) were also calculated. The trial initially included 69 patients (34 Gln, 35 placebo), but 11 patients were lost during follow-up (4 Gln, 7 placebo; P = 0.296). Chronic enteritis was developed by 14 % of patients: Gln 16.7 % versus placebo 11.1% (RR = 1.33; 95 % CI, 0.35–5.03; P = 0.540). Most cases of enteritis were grade I (75 %), with no differences between groups. The stool frequency increased after radiotherapy in patients who received Gln (from 1 ± 1 to 2 ± 2 stools per day, P = 0.012), but remained unchanged with placebo (1 ± 1 stools per day, P = 0.858; difference between groups P = 0.004). There were no differences between the two groups in terms of weight, fat mass, or fat-free mass index, or between patients with enteritis and those without intestinal toxicity. Chronic enteritis is a relatively infrequent phenomenon, and Gln administration during radiotherapy does not exert a protective effect. •Glutamine has been proposed as a nutrient with potential protective effects against the toxicity induced either by chemoradiotherapy, but few trials have studied this effect.•The administration of oral glutamine during abdominal radiotherapy was related with the development of gastrointestinal symptoms.•One year after finishing radiotherapy, the patients who received glutamine referred significant changes in stool frequency and characteristics.•Glutamine was not related to better nutritional outcomes compared with placebo.

Canine chronic enteropathy (CE) is a gastrointestinal disorder characterized by persistent or recurrent digestive symptoms lasting more than three weeks. It shares similarities with human inflammatory bowel disease but its immunopathogenesis remains poorly characterized in dogs. The aim of this study was to characterize the local and systemic immune profile of dogs with CE by assessing cytokine and chemokine expression in serum and intestinal tissue, as well as the mRNA expression of immune-related receptors such as integrins, chemokine receptors, and cytokines. Duodenal biopsies and blood samples were collected from five dogs diagnosed with a CE and five healthy controls. Serum concentrations of cytokines and chemokines were determined by multiplex ELISA, and mRNA expression in the intestinal mucosa was analyzed by quantitative PCR. Dogs with a CE showed increased expression of pro-inflammatory cytokines, including TNF-α and IFN-γ, and increased concentrations of chemokines such as CXCL10 and CCL2 in both serum and tissue samples. Increased mRNA expression of the chemokine receptor CCR9 and the adhesion molecule MAdCAM-1 were also observed in intestinal samples. These findings provide new insights into the immune response involved in CE and may aid the development of future diagnostic biomarkers and targeted therapies for canine chronic enteropathies.